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Head Trauma Dementia
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INTRODUCTION
Background: Prolonged or permanent changes in cognition, memory, emotions, or
behavior may follow head injury of any severity. The term post–head injury dementia
encompasses heterogeneous phenomena, reflecting the range of types and degrees of
head injury and the variety of patients who experience them.
The generic Diagnostic and Statistical Manual of Mental Disorders, Fourth edition
(DSM-IV) definition of dementia (ie, amnesia plus 1 of the following: agnosia, aphasia,
apraxia, or disturbance of executive function) provides a poor description of dementia
following head injury. This dementia usually is of the subcortical subtype. In subcortical
dementia, impairments of memory, language, praxis, and sensation are relatively less
prominent than in Alzheimer disease or other cortical dementias. Changes in
personality, disturbed executive functioning, and altered experience and expression of
emotion are relatively more apparent.
Broad as it is, the term post–head injury dementia fails to describe all the
neuropsychiatric sequelae of brain trauma. Head injuries may damage almost any brain
structure. They may be psychologically traumatic, and they precipitate major life
changes. Consequently, almost any psychiatric symptom or syndrome may follow head
injury. The DSM-IV allows for diagnoses of psychotic disorder, mania, major
depression, anxiety disorder, or personality changes secondary to head injury.
Adjustment disorders and posttraumatic stress disorder also may develop.
Other clinically important patterns of neuropsychiatric impairment after head injury
include the following:
Posttraumatic amnesia
Posttraumatic amnesia (PTA) describes the mental state of patients immediately
following closed head injury (CHI) or after awakening from coma. PTA is a form of
delirium that may persist for hours to weeks or, occasionally, months. Patients with PTA
are alert and capable of complex behavior. However, they experience severe memory
problems, feelings of confusion, inability to learn new information, and poor
concentration. PTA sometimes involves peculiar alterations of consciousness and selfawareness. As a measure of injury severity, the duration of PTA has prognostic
significance.
Posttraumatic thalamic syndrome
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Injury to the thalamus following CHI produces posttraumatic thalamic syndrome. In this
condition, the person progresses from generalized numbness to episodes of
spontaneous pain or pain in response to nonnoxious stimuli. Patients also experience
constant or episodic unpleasant sensations (burning, freezing, crushing, formication),
paresthesias, outbursts of fear or anger, aphasia, abusive behavior, and signs of frontal
lobe dysfunction.
Second injury syndrome
The second injury syndrome (SIS), although rare, is important as a cause of
preventable sudden death. SIS occurs when someone not yet fully recovered from a
head injury experiences another head or upper body injury, even seemingly trivial injury.
After a brief delay, the person suddenly loses consciousness. Signs of brainstem
compression follow, leading to death or permanent coma. The syndrome typically
affects young men who participate in rough sports. The mechanism may be failed
cerebral autoregulation, with subsequent engorgement of the brain vasculature.
Postconcussive or postconcussional syndrome
The manifestations of postconcussive or postconcussional syndrome (PCS) include
irritability, fatigue, headaches, dizziness, sensitivity to noise, cognitive slowing, memory
impairment, poor concentration, sadness, and anxiety.
While other sequelae of head injury are widely accepted as primarily neurological, PCS
falls between the domains of psychiatry and neurology. The syndrome follows mild-tomoderate CHI and produces significant disability. PCS is fairly rare in head injury that is
more serious. It has variable manifestations that do not correlate well with tissue injury,
and it shares many features with illnesses that are strongly influenced by psychological
and social factors. The onset of the syndrome may reflect injury to white matter (axons)
in the brain or brain stem injury. Persistence beyond 3-6 months seems related to the
patient’s ability to cope with his or her impairments and other psychosocial factors, in
addition to ongoing effects of tissue injury.
Pathophysiology:
Penetrating head trauma causes both focal damage and diffuse injury from bruising or
infection, if these occur. The diffuse aspects of penetrating injuries resemble those of
CHI.
The pathophysiology of CHI results from contusions and diffuse axonal injury (DAI).
Contusions are most common where the brain contacts with bony protuberances of the
skull. Typically, these are the basal areas of the frontal, temporal, and occipital lobes.
Contusions may occur at the site of impact (coup) or at the opposite pole of the brain
(contrecoup).
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DAI occurs in high-velocity trauma, especially trauma with an element of twisting or
rotation. The shearing forces of impact cause axons to stretch and break. Disruption of
axons triggers a cascade of further insults, including calcium influx, excitotoxin release,
phospholipase activation, and lipid peroxidation.
DAI, by definition, affects white matter. In dementia from white matter injury, cognitive
impairment is mild and progresses slowly. Personality remains relatively intact unless
other brain areas also are affected. When damage is extensive, patients experience
subcortical dementia, with bradyphrenia (slowing of cognition), bradykinesia, avolition,
mood changes, and motor abnormalities, with little apraxia, agnosia, or aphasia. Other
pathophysiologic processes that may follow head injury include subdural, epidural, or
intracerebral hematomas; hydrocephalus; and epilepsy, especially partial complex
epilepsy.
Posttraumatic epilepsy occurs mainly after penetrating head injuries, which cause
scarring and gliosis, creating epileptic foci. A seizure focus in the temporal lobe or other
part of the limbic system may trigger partial complex seizures. Psychopathology and
cognitive impairment are common in partial complex seizure disorders. Posttraumatic
epilepsy is not a form of dementia, although it may be a complicating factor.
Regarding pathophysiology, specifically of dementia after head injury, the pattern of
symptoms reflects the nature of the injury and the location of tissue damage. Symptoms
related to particular brain areas include the following:
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Prefrontal cortex - Disinhibition, apathy, personality change (coarsening,
flattening), decreased fluency of speech, obsessions, hypochondria, delusions
Basal ganglia - Depression, mania, tremor, cogwheeling, bradykinesia,
obsessions, compulsions
Thalamus - Apathy, irritability, pathological crying, paresthesias, pain,
hypersomnia
White matter - Apathy, lability, loss of spontaneity, transient hemiparesis or
hemiplegia, bradykinesia, bradyphrenia
Cerebellum/pons - Mild avolition, disinhibition, cerebellar signs, loss of ability to
execute motor routines automatically
Frequency:
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In the US: Persistent neuropsychiatric impairment following head injury is a
significant public health problem. Military populations are especially prone to
penetrating injuries, with relatively more CHIs occurring in civilian populations.
From 400,000-500,000 people are hospitalized in the United States every year
for head injury; many more people are injured and do not require admission.
Head injury is the third most likely cause of dementia, after infection and
alcoholism, in people younger than 50 years. The overall incidence of traumatic
brain injury is roughly 200 cases per 100,000 population.
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Internationally: No information is available.
Mortality/Morbidity: Patients who display dementia or PCS following head injury have
survived the risk of mortality from head injury itself. Estimates of morbidity vary widely,
depending on criteria for both significant trauma and classification of impairment. The
morbidity of penetrating head injury reflects the site of brain injury and degree of
associated complications, especially infections and contusions (early complications) and
seizures (later complications).
Morbidity from CHI is variable and difficult to predict. Most estimates of morbidity stratify
populations into those with mild, moderate, or severe injury, based on their scores on
the Glasgow Coma Scale (GCS) and the duration of PTA. By definition, mild injury
entails less than 15 minutes of unconsciousness (GCS > 13) or less than 1 hour of PTA
in the absence of skull fracture. PTA of less than 1 hour predicts full recovery, while
PTA of greater than 24 hours in adults predicts neuropsychiatric disability.
Between these benchmarks, the prognosis of an injury varies from complete recovery to
persistent symptoms and disability. In 1968, a study by Lishman of 670 patients with
either closed or penetrating head injuries yielded the following relationships between
PTA and psychiatric disability or cognitive impairment.
The numbers may have changed somewhat since 1968 due to improved survival and
better means of assessment. Nevertheless, these data describe relationships that
remain valid. Although severity of head injury as measured by depth of coma and length
of PTA correlates with long-term sequelae, mild injuries sometimes lead to severe
impairment and disability. Conversely, not all severe injuries have severe
consequences. Other factors that predict morbidity include patient age, history of prior
injury, history of alcohol use (especially at time of injury), location and extent of focal
brain damage, degree of DAI, evidence of brain stem dysfunction at the time of injury,
and psychosocial adversity before or following injury.
The factors related to injury severity correlate most strongly with problems of memory,
cognitive slowing, and impaired information processing. They contribute to mood,
personality, and behavioral sequelae to an immeasurable degree. Psychosocial
adversity and stress also contribute to the morbidity of post–head injury dementia and of
PCS.
Race: No relevant information is available.
Sex: Men predominate over women in the population of persons experiencing head
injury.
Age: Head injuries and their sequelae are most frequent in males aged 14-24 years.
However, patients who are middle-aged or older are likely to have sequelae that are
more persistent. Very young children with head injuries also have worse outcomes.
CLINICAL
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History: The clinical picture of post–head injury dementia includes features of
subcortical dementia (see Background). These manifestations persist after the
resolution of PTA. They may improve steadily over 6 months and more gradually over 2
years. Late, partial resolution of impairment and disability after 5 years is possible, even
in people with persistent impairment after 2 years. Such improvement may reflect
continued tissue healing, benefits of prolonged rehabilitation, or both.
The natural history of PCS follows a time course somewhat similar to that of dementia
from head injury. Rapid improvement typically occurs within the first 6 months.
However, impairments may persist a year or more. Headache, dizziness, memory
impairment, and fatigue are present in 30-50% of people during the first month after a
mild head injury. In a recent prospective study of mild CHI conducted in Belfast, these
symptoms disappeared within 6 months in 52% of cases and persisted in 16%. Thirtytwo percent of survivors reported a worsening of symptoms between 6 weeks and 6
months. Other studies report improvement continuing as long as 2 years, then reaching
a plateau.
Cognitive difficulties, including slowed processing of information, decreased attention
span, and decreased memory, may resolve within 3 months or persist, especially in
elderly people.
Cross-sectional studies demonstrate that many PCS symptoms are common in agematched controls. However, as many as 80% of head injury survivors have symptoms
of headache and dizziness at levels greater than uninjured controls a year or longer
after the event.
While the injury itself contributes heavily to initial and persistent symptoms, worsening
of symptoms over time relates to patients’ levels of anxiety, depression, and social
adversity. Anxiety and depression, in turn, relate both to psychological coping and to
brain stem injury.
Significant functional impairment, marked by unemployment and marital dysfunction,
typically accompanies PCS. In research populations, involvement in litigation plays a
relatively small role in either the genesis or the resolution of patients’ complaints.
 Patients treated for sequelae of head injury should be screened for the
development or recurrence of any major psychiatric syndrome, with specific
screening for the following:
o Depression
o Anxiety
o Mania
o Psychosis
o Obsessive-compulsive symptoms
o Impulsivity
o Suicide risk
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Standard rating scales, especially the Hamilton Depression Rating Scale and the
Positive and Negative Symptom Scales, allow for reliable measurement of
symptom severity.
Also inquire about subsyndromal complaints and nonspecific somatic distress,
especially fatigue and headache. These, along with irritability, anxiety, apathy,
and dysphoria, are cardinal features of PCS. Seizure phenomena, especially
partial-complex seizures, should be explored specifically.
The nature and severity of head trauma affect the nature and severity of
sequelae. Obtain information from patients and usually from their hospital
records about the injury, the immediate sequelae, and the medical treatment
received. Specifically, the clinician needs to know if the injury included a brain
contusion, whether the impact was forward and back or involved some degree of
rotation, the patient’s score on the GCS, and the duration of PTA. Patients may
provide an estimate of their PTA, or the record may include a rating on the
Galveston Orientation and Amnesia Test (GOAT). Each of these aspects of head
trauma contributes to persistent sequelae.
Evaluation for dementia per se requires close attention to cognitive symptoms,
including subjective complaints concerning memory, concentration, and speed of
processing and more objective measures. Testing for aphasia and apraxia are
important in head injury, along with evaluation of retention, short-term memory,
and abstraction. Although it tests these functions, the Mini-mental State
examination may not be sensitive to the degree of impairment observed after
head injury, which may be less than in Alzheimer-type dementia.
Neuropsychological testing is the most sensitive means of characterizing the
cognitive deficits of survivors of head injury. Clinical rating scales, such as the
Ranchos Los Amigos Cognitive Scale and the Neurobehavioral Rating Scale,
allow clinicians to identify some subtle impairments and establish clear baselines
against which to measure change.
The social/developmental history provides important information. Many survivors,
especially those with significant impairment, have experienced more than one
head injury. Substance abuse is a common contributor to head injuries from car
accidents, violence, and falls. Both prior and current substance abuse adversely
affect prognosis. Perceived high stress immediately prior to injury seems to
contribute to adverse outcomes. Perceived stress after injury complicates
recovery and rehabilitation.
The clinician needs to know, in particular, if the patient is involved in litigation
related to the injury. Legal proceedings may have an impact on patients’ ability to
ignore symptoms, their motivation to participate in rehabilitation, and their
affective state. In addition, knowing at the outset if legal reports of treatment will
be required is important.
Physical: A thorough and careful neurologic examination should include special
attention to the following:
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Head Trauma Dementia
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Cranial nerves: Anosmia stems from damage to the olfactory tracts, confirming
injury to the limbic system. Visual-field mapping may identify damage to the optic
nerves. Nystagmus may reflect subtle labyrinth injury.
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Weakness: Hemiparesis may reflect DAI.
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Cerebellar signs include dysmetria and nystagmus.
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Signs of parkinsonism, including tremor, cogwheeling, and abnormal gait, confirm
damage to the basal ganglia.
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Mental status examinations should be conducted repeatedly on patients with
sequelae of head injury, with particular attention to the cognitive sections. Careful
documentation is important to describe baseline function and to follow changes
over time, especially if the patient is involved in legal proceedings. The typical
mental status examination includes the following sections:
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Appearance: Especially note grooming and adventitious or abnormal
movements.
Level of consciousness: Note whether the patient is alert or fluctuating.
Affect: Note whether affect is appropriate or labile, blunted, or flat.
Mood: Patients may be euthymic, depressed, anxious, or angry.
Thought form: Note whether thought form is organized instead of
disorganized, circumstantial, or tangential. Note especially paucity of
content, blocking, or perseveration.
Cognitive functions: Note orientation to person, place, and time.
Concentration/attention: Assess the patient’s ability to repeat digits
forward and backward (note number of digits). A healthy person should be
able to remember 7 digits forward and 5 in reverse. Ask the patient to
perform serial subtractions of 7 from 100, down to 44. Note accuracy and
if patient seems unduly slow.
Memory: Give the patient 3 unrelated objects and ask for immediate
repetition (registration). Test the patient’s ability to recall the objects after
3 or 5 minutes (retention/short-term memory).
Long-term memory: Elicit details of personal history from the patient.
Aphasia
 Assess whether the aphasia is nominative/dysfluent. Ask the
patient to name 3 objects or parts of objects.
 Conduction: Ask the patient to repeat the phrase "no ifs, ands, or
buts about it."
 Receptive/fluent: Assess the patient’s ability to understand and
follow commands.
Apraxia: Ask patient to copy a drawing.
Other cortical functions (sequencing): Have the patient follow a 3-step
written command.
Agnosia: Ask the patient to name a common object placed in the palm.
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Judgment: Assess recent history. Have the patient respond to standard
test questions. The following are examples. What would you do if you
found a stamped letter lying in the street? What would you do if you woke
up with very severe pain in your chest?
Abstraction: Have the patient identify the similarity between common
objects.
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Patients with mild-to-moderate post–head injury dementia should be consistently
alert.
o They may show poor or eccentric grooming; bradykinesia or restlessness;
labile or blunted affect; and shallow, often dysphoric, mood.
o Other abnormal findings that would be typical include remembering 1, 2,
or 3 objects after 5 minutes; digit span less than 6 forward, 4 in reverse;
slow serial subtractions with computative errors; some difficulty with a 3step command; and concreteness or perseveration.
o Occasionally, patients with marked frontal lobe impairment make
inappropriate jokes or puns.
o In contrast to Alzheimer dementia, nominative aphasia, apraxia, and
agnosia are not prominent, although slow retrieval of words may occur.
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A patient with PCS also should be alert.
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More typically, they are well groomed.
These patients may have obvious anxiety, sadness, or irritability, and may
seem more focussed on having their deficits acknowledged, compared to
someone who is more demented.
Short-term memory, cognitive speed, and concentration may be
somewhat reduced.
Findings from the remainder of the mental status examination, including
thought form, abstraction, praxis, and speech, should not be markedly
impaired.
Causes:
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Causes of head injury in civilian populations include the following:
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Car accidents (50%)
Falls (21%)
Assault (12%)
Recreational activity (10%)
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Roughly 50% of these injuries are associated with alcohol use.
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In children, bicycle accidents are a significant cause of head injury.
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Among infants, most injuries reflect child abuse.
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Elderly patients are especially vulnerable to falls.
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Increased survival following severe injury contributes to the increasing overall
number of people in need of treatment for late sequelae.
DIFFERENTIALS
Other Problems to be Considered:
Differential or comorbid diagnoses of dementia
Subdural hematoma
Epidural hematoma
Hydrocephalus
Partial complex epilepsy
Primary or secondary psychotic disorder, mood disorder, anxiety disorder, or personality
change
Differential or comorbid diagnoses of postconcussional syndrome
Major and minor depression
Adjustment disorders
Mixed anxiety depression (demoralization)
Conversion disorder
Malingering
Posttraumatic stress disorder
Other anxiety disorders
Apply the diagnoses of conversion disorder and malingering with great caution in
survivors of head injury. The head is fraught with symbolic significance, inviting the
expression of conflict or inexpressible feelings through pseudoneurologic symptoms.
However, many symptoms previously considered hysterical or manifestations of
conversion disorder now are recognized as elaborations of organic deficits that
previously were undetectable.
Many head injuries occur in situations that may lead to litigation and compensation, a
source of motivation for secondary gain. Dissatisfaction with a work or family situation
also may prompt a person to magnify or create symptoms after a head injury. However,
caution is warranted. Involvement in litigation does not reliably predict the severity or
extent of symptoms after head injury. Settlement of pending lawsuits also does not
cause resolution of symptoms.
WORKUP
Imaging Studies:
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Other than collecting hospital records and neuropsychological testing,
specialized workup may require the following:
o Sleep-deprived electroencephalogram can be used to diagnose seizures.
o CT scan performed 1-3 months after injury may detect cerebral contusions
not visible immediately.
o MRI scans are more sensitive than CT scans in demonstrating DAI and
frontal and temporal lesions.
o Single-photon emission computed tomography (SPECT) scan is a
relatively accessible form of functional imaging that, in the future, may
prove the most sensitive measure of white matter lesions. Further
research is needed to correlate such lesions with their clinical effects.
Other Tests:
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Neuropsychological testing is the most reliable way to document and quantify
cognitive impairments following head injury.
Histologic Findings: The pathophysiology of CHI results from contusions and DAI. DAI
occurs in high-velocity trauma, especially trauma with an element of twisting or rotation.
The shearing forces of impact cause axons to stretch and break. Disruption of axons
triggers a cascade of further insults, including calcium influx, excitotoxin release,
phospholipase activation, and lipid peroxidation.
Staging: Head injury severity is rated based on the GCS and the GOAT results.
Severity of sequelae may be rated on the Ranchos Los Amigos Cognitive Scale or the
Neurobehavioral Rating Scale.
TREATMENT
Medical Care: This article does not discuss the treatment of patients with acute head
injury during the period of coma and PTA.
Both the patient who has become demented and one who has developed PCS benefit
from psychological support and education with the following, when indicated: (1)
behavioral modification, (2) cognitive rehabilitation, (3) psychotropic medication for
specific syndromes or symptoms, (4) family or network intervention, (5) social services,
and (6) medical support in legal proceedings.
Psychological intervention with patients with head injuries shares the goals of all
psychotherapy—instilling and maintaining hope, supporting mastery, and helping the
patients arrive at an adaptive meaning for their experience. Patients benefit from a
sustained relationship with a knowledgeable physician or treatment team, regardless of
the severity of the brain damage. Therapy involves helping patients and their families be
realistic about their losses and impairments, while encouraging hope and continued
effort in rehabilitation. Helping patients and caregivers to interpret subtle and disruptive
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changes in personality in light of organic damage is particularly important to relieve guilt
and blame.
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Psychological support
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Head injuries often precipitate an abrupt deterioration of general
adaptation. Sudden adverse change inevitability produces anxiety, which
may lead to demoralization or depression. In the case of head injury,
damage to the brain impairs the person’s ability to cope at a time when the
need to adapt is greatest. The fact that patients with head injury are more
distressed than those who experience equally disabling injuries to other
parts of the body is not surprising.
The meaning of any injury varies in part based on the patient’s prior
concerns and personality. For example, narcissistic patients feel
narcissistically wounded by even minor losses of function. Prior emotional
lability or capacity for aggression in a patient who is borderline may
worsen following a head injury.
Injury when a person is in transition or moving towards an important goal,
such as marriage, school completion, or job performance, has a different
meaning than injury occurring when someone feels stable, stagnant, or
deteriorating. Injuries that occur on a job a person already dislikes or
injuries that result from negligence may evoke resentment and feelings of
entitlement that are absent in similar injuries in other circumstances.
Understanding the person’s preinjury personality, stresses, and the
circumstances of the injury help establish realistic goals and minimize
stress during rehabilitation and reentry into life. Interpreting the person’s
reactions to injury in light of his or her previous state builds trust, reflecting
the degree to which the patient feels understood and accepted.
Avoid interpreting changes in personality or behavior in light of
developmental issues or conflicts without considering the impact of the
injury itself. Such interpretations may produce confusion, guilt,
unnecessary resentment, and fatalism. A present-oriented, problemfocussed therapy generally is best for patients after head injury, even
those whose impairment appears to be driven by exaggerated emotional
responses to the experience.
Different stages of recovery require different types of psychological
support. In the first months after injury, validating symptoms, helping
patients relinquish responsibilities, mourning losses of function or hopes,
and counseling patience with the pace of improvement are critical. Later,
patients may need encouragement to push themselves to regain selfconfidence and reassume their previous roles and responsibilities.
Behavior modification
o Research on patients who are severely impaired and who are treated in
specialized units supports the value of behavior modification. Behavioral
techniques may be used to discourage impulsivity, aggression, and
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socially inappropriate behavior. They also may encourage patients to be
less apathetic or withdrawn. In any case, desired behaviors are reinforced
with attention or specific rewards such as tokens for privileges.
Undesirable behaviors provoke withdrawal of attention. Sometimes,
specific techniques such as time-out or isolation from others may be used.
o Teaching sleep hygiene is a behavioral intervention for insomnia. When
effective, sedative medication may be used with caution in patients with
head injury, due to their sensitivity to adverse effects.
o Patients with simple PCS are not treated in hospital-based behavior
programs, impeding research in this area. However, families can learn
behavioral approaches that may benefit this group. Anxiety, loss of selfconfidence, and intolerance of stimulation all seem ripe for behavioral
interventions. While the line between impairment and exaggerated illness
behavior is hard to draw, using concrete and immediate rewards to
encourage the highest functioning of which patients seem capable is a
sound therapeutic principle.
Cognitive rehabilitation
o Psychologists with special training typically conduct cognitive rehabilitation
programs. The underlying principles are encouraging recovery in functions
that are capable of improvement, compensation for areas of fixed deficit,
and teaching substitute means of achieving particular ends. For example,
gradually increasing time spent reading helps a patient both regain
concentration and develop confidence in his or her ability to concentrate.
Keeping lists allows a patient to compensate for decreased memory.
Someone who has become dysarthric or aphasic may learn sign language
as a substitute means of communication.
o In general, cognitive rehabilitation is based on neuropsychological testing
that clarifies deficits and suggests areas of preserved functioning in
patients with dementia. Patient with PCS also have cognitive complaints,
usually decreased attention and concentration. These symptoms may
reflect slowly or partially reversible damage to white matter from DAI.
Decreased attention and concentration seriously worsen anxiety and
otherwise compromise patients’ efforts to recover. When impaired
concentration and attention are prominent in a patient with PCS, cognitive
rehabilitation may be quite helpful.
Family or network intervention
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The changes in personality, especially apathy, irritability, and aggression,
in patients with head injury are especially burdensome to caregivers,
family, or professional care providers. Head injuries cause more family
distress than bodily injuries of equivalent severity. Counseling for
caregivers is essential. When the patient is demented, interpreting
impairments as organic and insisting on the legitimacy of the sick role are
needed to relieve blame and guilt.
Even when the caregiver understands the person’s behavior is not within
his or her control, the patient’s slowness, inappropriateness, and erratic
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responsiveness can be exasperating or even frightening. Family members
become isolated from usual support, especially when the person’s
impairments are severe, protracted, or fixed. Direct communication
between the caregiver and the physician allows caregivers to vent their
feelings and voice their concerns. Problem-solving interventions and
referral to support groups for family members improve morale and
enhance patient outcome. Regular staff or team meetings sustain morale
in professional caregivers.
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Social services
o Case management for patients with dementia sometimes is necessary to
help patients apply for disability, locate specialized rehabilitation
programs, attend to medical problems, and participate consistently in
treatment.
o When people have prominent severe problems of information procession
or frontal lobe deficits manifested by impulsivity and poor judgment, they
may be incompetent to make medical decisions or handle their own
affairs. These 2 functions may differ. Guardianship, conservatorship, or
some other protective legal arrangement may be needed. Physician
evaluation typically is required, unless the person is competent enough to
sign a power of attorney or designate a substitute payee.
Medical support in legal proceedings
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Head injuries often occur in the context of car or workplace accidents,
leading to legal proceedings for damages and compensation. The
prognosis of mild or moderate dementia and PCS remain difficult to
provide with certainty. Some patients recover fully from severe injuries
with prolonged coma, others remain disabled for long periods after much
milder insults. Moreover, involvement in legal proceedings seems to
complicate recovery. Having to repeat the story of an injury to questioners,
not knowing what expenses will be incurred and which will be covered by
insurance, and proving the reality of subtle impairment without visible
scars increase patients’ stress and anxiety. Stress seems to slow or
impede recovery by both psychological and physiological mechanisms.
Malingering also may occur.
Physicians caring for patients with head injuries should anticipate having
to testify in depositions or court proceedings. They must clearly document
impairment and objective findings, quantifying symptoms and progress in
recovery whenever possible. Standard symptom rating scales, such as the
symptom checklist 90 (SCL-90) or the Hamilton rating scales for anxiety
and depression and the Positive and Negative Symptoms Scale may be
used for appropriate patients. The Ranchos Los Amigos Cognitive Scale
and the Neurobehavioral Rating Scale are especially sensitive to the
particular symptoms of patients with head injury. Physicians should order
neuropsychological testing to validate clinically suspected impairments
that may be difficult to prove in face-to-face interaction.
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o
When called to testify, be aware of personal attitudes towards patients
who are dependent, not improving quickly, not functioning to their ability,
or expressing undesirable attitudes of resentment or entitlement. None of
these factors should blind the physician to the reality of patients’ distress
and impairment. Testifying for either the defendant or the plaintiff in a
head injury case requires honesty, humility, and awareness of the
uncertainty surrounding the causes and the outcomes of the symptoms
that patients develop.
Consultations:
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Consultations with neuropsychologists and physical and occupational therapists
are helpful in designing or altering the long-term treatment plan of a patient with
head injury.
Neurological consultation is essential to diagnose and treat seizures, subdural or
epidural hematomas, or hydrocephalus. Neurologists also may help with the
management of headaches, dizziness, or fatigue.
Consult primary care physicians to ensure that concurrent medical conditions are
not neglected.
Diet:
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Patients with impairment in their ability to prepare food or feed themselves must
have their diets monitored to be sure that they do not become malnourished or
vitamin deficient.
Otherwise, no special dietary prescriptions or restrictions apply.
Activity:
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In the early phases of rehabilitation, simple, graduated physical exercises and
games may improve endurance and self-confidence. Head injuries may lead to
ataxia, parkinsonism, hemiparesis, or paraparesis, requiring mobility aids and
monitoring. In elderly patients, altering the environment to prevent falls is
important to prevent repeat injuries.
Recommending that patients resume normal activities or responsibilities is not
always simple. Patients who work night-shift jobs, work with heavy machinery,
work off the ground, or who are in overstimulating environments may not be able
to return to their previous positions. Returning to work when cognitive
impairments are in flux may lead to failure and regression in recovery. However,
patients also may be unduly reluctant to return to previous activities for fear of
further injury, embarrassment about their disabilities, and underestimation of their
competence. Encouraging gradual return to work or requesting temporary
accommodations that allow patients to relearn or reacclimate to their jobs often is
helpful, although not always possible.
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
Finally, patients who play contact sports should not be allowed to return to play
until their concussive symptoms have resolved completely. Failure to observe
this restriction exposes these patients to the risk of sudden death from SIS.
MEDICATION
Patients with head injury may require treatment with psychotropic medication for
depression, mania, psychosis, aggression, irritability, emotional lability, insomnia,
apathy, or impaired concentration. Headaches also may respond to
psychopharmacologic treatment.
Brain damage renders patients more sensitive to adverse anticholinergic effects,
seizures, and drug-induced parkinsonism. Doses in the usual therapeutic range may be
needed to relieve target symptoms, especially for depression and mania; however,
initiate at lower doses and titrate upward more slowly than in other patients under
psychiatric care.
Dopamine-blocking agents (eg, haloperidol) and adrenergic-blocking agents (eg,
clonidine, prazosin) compromise brain tissue repair in animal laboratory models.
Dopamine-potentiating agents (eg, dextroamphetamine) enhance recovery in animal
models. These effects have not been documented in humans with head injury, although
alpha-blockers, haloperidol, and benzodiazepines may adversely affect functional
outcome after strokes.
Drug treatments for patients with brain injury are extrapolated from studies of patients
after stroke or other types of brain damage. These patients may not be comparable to
patients with head injuries, especially those with DAI. Clinical trials in patients with head
injury typically are small. No broad consensus or established guidelines exist regarding
psychotropic drug treatment after head injury.
Specific target symptoms and appropriate medications include the following:




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



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Depression - Selective serotonin reuptake inhibitors (SSRIs), nefazodone,
bupropion, nortriptyline
Insomnia - Trazodone, nefazodone
Mania - Valproic acid, carbamazepine, lithium
Emotional lability (eg, pathological laughing, crying) - Bromocriptine, nortriptyline,
fluoxetine
Psychosis -Olanzapine, risperidone, haloperidol
Hypoarousal - Dextroamphetamine, methylphenidate
Poor concentration (eg, apathy, fatigue) - Methylphenidate, bromocriptine,
amantadine, levodopa and carbidopa (improvement may not be sustained)
Chronic aggression and irritability - Antiepileptic drugs, SSRIs, olanzapine
Headaches - Amitriptyline, nonsteroidal anti-inflammatory drugs (NSAIDs),
antimigraine drugs
Anxiety - Buspirone
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Acute agitation or aggression may be treated with benzodiazepines; however, first-line
treatment of chronic symptoms includes drugs having less sedative effects or impact on
cognition. Avoid phenobarbital for treating seizures due to sedation. Over-the-counter
anticholinergic hypnotics are not to be used for patients with head injury.
Drug Category: Antidepressants -- Treatment of depressive syndromes due to
traumatic brain injury. Indications include signs and symptoms of major depression with
or without psychosis, dysthymia, or adjustment disorder.
SSRIs are the antidepressants of choice due to minimal anticholinergic effects. All are
equally efficacious. The choice depends on adverse effects and drug interactions.
SSRIs also are used to treat behavioral disturbances resulting from head trauma.
Tricyclic antidepressants (TCAs) are used when unable to use SSRIs. Their unfavorable
adverse effect profile prompted development of newer antidepressants. Advantages
include ability to obtain blood levels, thus ensuring therapeutic response and avoiding
toxicity. Prior to initiating, obtain ECG and blood pressure.
Newer antidepressants useful for sleep disturbances include nefazodone and
trazodone. They are structurally unrelated to TCAs, tetracyclics, or MAOIs. Cardiac
conduction effects of trazodone are qualitatively dissimilar and quantitatively less
pronounced than TCAs and therefore are less toxic in overdose.
Drug Category: Dopaminergic agents -- Enhancing dopamine function may
improve concentration, attention, and interest in patients after head injury.
Dopaminergic drugs include bromocriptine, amantadine, and levodopa/carbidopa.
Animal studies demonstrate that dopamine function enhancement may have
neuroprotective effects. Bromocriptine combined with antidepressants has been used
for pathological emotional lability. The most potent dopaminergic drug is levodopa;
therefore, it also produces the highest toxicity . Other drugs should be tried first.
Stimulants (eg, dextroamphetamine, methylphenidate) also enhance dopamine function.
Stimulants and direct or indirect dopamine agonists affect dopamine pathways
differently, despite similar mechanisms of action.
Drug Category: Antipsychotic agents -- Treatment of hallucinations, ideas of
reference, delusional preoccupation, and agitation. Older antipsychotics with strong
anticholinergic adverse effects (eg, chlorpromazine, thioridazine) may worsen cognitive
function. Potent conventional antipsychotics (eg, haloperidol) have been used in
patients with dementia with psychotic symptoms. While these drugs are effective,
patients with brain damage are more susceptible to drug-induced parkinsonism.
Haloperidol produces high levels of parkinsonian symptoms and risk of irreversible
syndrome of tardive dyskinesia.
New antipsychotics (eg, risperidone, olanzapine) may be safer for demented patients
than older drugs, according to 2 recently published studies. Olanzapine may have
particular efficacy for agitation and psychosis in patients with Alzheimer disease and for
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cognitive symptoms in schizophrenia. This suggests that head injury patients also may
benefit from this drug. In these studies, the main adverse effects of olanzapine that
require special concern in dementia are somnolence and unsteady gait.
No atypical antipsychotics are available parenterally, a disadvantage when used to
control agitation or when administered on an involuntary basis.
Drug Category: Antiepileptic drugs -- Behavioral disturbances (eg, chronic
aggression, agitation) are severe complications of head injury. Pharmacological agents
used to treat these behaviors include antiepileptic drugs, SSRIs, and beta-blockers.
Drug Category: Mood stabilizers -- The mood stabilizer that is not an anticonvulsant
is lithium. Studies have demonstrated potential benefit of lithium for explosive and
violent behavior in patients with organic disorders. Double-blind placebo-controlled trials
conducted over 16 wk on violent adult prisoners, patients with mental retardation, and
patients with brain injury demonstrated decreased impulsivity and aggressive behavior.
Lithium levels during the trials were maintained at 0.7-1.0 mEq/L.
Drug Category: Benzodiazepines-- Used for rapid control of agitation in dementia.
They potentially worsen cognition; thus, their use in correcting sleep-wake cycle
disturbances or treating anxiety in this population is discouraged. Used primarily to
produce rapid calming needed for patients who are violent or agitated.
Drug Category: Beta-blockers -- Effective for treating aggression resulting from head
injury. They also are used for reducing restlessness and disinhibition. Treatment for
persistent agitation and aggression in organic brain syndromes.
Drug Category: Atypical antipsychotics -- See above.
FOLLOW-UP
Deterrence/Prevention:




Primary prevention of head injury involves the use of protective gear in contact
sports, seat belts, bicycle and motorcycle helmets, and hard hats in appropriate
jobs.
For elderly patients, altering the environment to minimize the risk of falls is
important.
Protecting children from child abuse helps prevent head injuries.
Patients who have had one head injury are at risk for others.
o Identification and treatment of substance abuse makes subsequent injury
less likely.
o Some patients with head injury are parasuicidal. They may benefit from
treatment of depression, character disorders, and other conditions
associated with suicide.
o Restricting return to play for athletes prevents SIS.
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
Prevention of sequelae in patients once they have been injured is an active area
of research. Recent reviews of the subject suggest hypothermia during the period
of coma may mitigate tissue damage. Prophylactic use of anticonvulsants is not
recommended.
Complications:
 Reactions to anticholinergic, analeptic, and parkinsonian adverse effects of
medication
 Subdural and epidural hematomas
 Hydrocephalus
 Partial complex or grand mal seizures
 Exacerbations of preexisting psychiatric disorders, including preexisting dementia
 Conversion symptoms
o Conversion symptoms typically occur when a person feels trapped in a
threatening situation, especially if he or she is unable to openly talk about
the dilemma with others who are trusted.
o Patients with head injury often face such dilemmas, being forced to return
to work when they feel unable, being expected to perform normal family
roles despite significant problems of cognition or mood, and being subject
to hostile legal scrutiny. Moreover, the head is a symbolically significant
part of the body. For all of these reasons, some of the nonspecific distress
of patients with head injury and, more rarely, some of their focal
complaints may be understood as conversion symptoms or somatization.
Prognosis:

The prognosis of mild or moderate dementia and PCS remains difficult to provide
with certainty. Some patients recover fully from severe injuries with prolonged
coma; others remain disabled for long periods after much milder insults.
Patient Education:

Patients with dementia
o
These patients need simple explanations of their impairments. While they
may be aware of cognitive dysfunction, they may lack insight into
impairments in judgment, changes in personality, elevated mood, or
paranoid symptoms. Education should include the expected course of
improvement, with the greatest improvement expected in the first 6
months but delayed improvement possible as long as 5 years after injury.
o
Caretakers of patients with dementia need a great deal of ongoing
education and support. Importantly, the patient's environment must be
neither tedious nor overstimulating. Maintaining consistent routines of light
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and dark, eating, sleeping or lying in bed, performing bathroom activities,
and participating in therapeutic or recreational activities help patients
remain emotionally balanced and minimize caregiver burden.

o
Keeping the environment safe by eliminating area rugs to reduce falls,
providing tub bars, and putting child locks on cabinets or stove knobs also
is important in the care of patients with dementia. If the patient is capable
of going out alone, the caregiver should ensure that he or she knows the
routes well, carries identification, wears a medic alert bracelet, and knows
how to use phones (especially cell phones) and busses.
o
Caregivers for patients with mild dementia need to decide whether the
person should continue to have access to checking accounts or credit
cards. If the person is willing and competent, the caretaker should
consider getting power of attorney, in order to monitor the person's use of
financial resources. If the patient has markedly poor judgment or seems
seriously incompetent, the caregiver should seek formal conservatorship,
to have legal authority to manage the person's resources.
o
Caregivers should be included in the patient's relationship with health care
professionals. They should be specifically told to seek help if the patient
has very disrupted sleep; does not eat a balanced diet; or is incontinent,
aggressive, or sexually inappropriate. Any marked change in behavior
should prompt a call to the clinician. Because patients with dementia do
not always show typical symptoms when acutely ill, taking the patient's
temperature and looking for signs of infection is a particularly important
step if the patient shows a change.
o
Clinicians, in turn, must be accessible to caregivers. Meeting with more
than one family member to stress the importance of having family
members and friends share the burdens of providing care often is an
overlooked step. Although one particular friend or relative may know the
most about a patient and assume most of the responsibility, sharing this
with others reduces the likelihood of the caregiver becoming isolated or
depressed, an otherwise common outcome of providing long-term family
care.
Patients with postconcussional syndrome
o
Patients with PCS need to know that headaches, dizziness, fatigue,
irritability, poor concentration, and decreased memory are common in the
first 3-6 months after injury. These symptoms fully resolve in most patients
after mild injury. However, persistent impairment is possible. Patients
should know that anxiety, depression, decreased concentration, and other
persistent symptoms may improve with rehabilitation, psychological
support, and medication.
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o

Caregivers need to adopt a posture of encouragement and expectation
that the patient will try to be as independent and productive as possible. At
the same time, caregivers need to be patient and tolerant. They should
accept that the patient may have real limitations and that these will likely
worsen if the person is tired, ill, or acutely stressed. Emphasizing what the
person can still do, rather than what seems to be lost, generally is helpful.
The traumatic brain injury page of the National Institutes of Health contains links
to other organizations providing education and support.
MISCELLANEOUS
Medical/Legal Pitfalls:

In treating patients with head injuries, the physician needs to know if the patient
is involved in litigation related to the injury.
o Anticipate having to testify in depositions or court proceedings.
o Document impairment and objective findings clearly, quantifying
symptoms and progress in recovery whenever possible.
o When called to testify, be aware of personal attitudes towards patients
who are dependent, not improving quickly, not functioning to their ability,
or expressing undesirable attitudes of resentment or entitlement. None of
these factors should blind the physician to the reality of patients’ distress
and impairment. Testifying for either the defendant or the plaintiff in a
head injury case requires honesty, humility, and awareness of the
uncertainty surrounding the causes and the outcomes of the symptoms
that patients develop.

Involvement in litigation does not reliably predict the severity or extent of
symptoms after head injury. Settlement of pending lawsuits also does not cause
resolution of symptoms.

When people have prominent severe problems of information procession or
frontal lobe deficits manifested by impulsivity and poor judgment, they may be
incompetent to make medical decisions or handle their own affairs.
Guardianship, conservatorship, or some other protective legal arrangement may
be needed. Physician evaluation typically is required, unless the person is
competent enough to sign a power of attorney or designate a substitute payee.
REFERENCES

American Academy of Neurology: Assessment of brain SPECT. Report of the
Therapeutics and Technology Assessment Subcommittee of the American
Academy of Neurology. Neurology 1996 Jan; 46(1): 278-85.
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American Psychiatric Association: Diagnosis and Statistical Manual of Mental
Disorders. 4th ed. Washington, DC: American Psychiatric Association Press;
1994.
Bohnen N, Jolles J: Neurobehavioral aspects of postconcussive symptoms after
mild head injury. J Nerv Ment Dis 1992 Nov; 180(11): 683-92.
Cantu RC: Return to play guidelines after a head injury. Clin Sports Med 1998
Jan; 17(1): 45-60.
Erlanger DM, Kutner KC, Barth JT: Neuropsychology of sports-related head
injury: Dementia Pugilistica to Post Concussion Syndrome. Clin Neuropsychol
1999 May; 13(2): 193-209.
Frank JB, Degan D: Conservatorship for the chronically mentally ill: review and
case series. Int J Law Psychiatry 1997 Winter; 20(1): 97-111.
Frank JD, Frank JB: Persuasion and Healing: A Comparative Study of
Psychotherapy. 3rd ed. Baltimore, Md: Johns Hopkins University Press; 1991.
Gasquoine PG: Postconcussion symptoms. Neuropsychol Rev 1997 Jun; 7(2):
77-85.
Jacobson RR: The post-concussional syndrome: physiogenesis, psychogenesis
and malingering. An integrative model. J Psychosom Res 1995 Aug; 39(6): 67593.
Lishman WA: Head Injury. In: Organic Psychiatry: The psychological
consequences of cerebral disorder. Malden, Ma: Blackwell Science; 1998: 161217.
Liss M, Willer B: Traumatic brain injury and marital relationships: a literature
review. Int J Rehabil Res 1990; 13(4): 309-20.
Macciocchi SN, Reid DB, Barth JT: Disability following head injury. Curr Opin
Neurol 1993 Oct; 6(5): 773-7.
McAllister TW: Neuropsychiatric sequelae of head injuries. Psychiatr Clin North
Am 1992 Jun; 15(2): 395-413.
Nuwer M: Assessment of digital EEG, quantitative EEG, and EEG brain mapping:
report of the American Academy of Neurology and the American Clinical
Neurophysiology Society. Neurology 1997 Jul; 49(1): 277-92.
Robertson A: The post-concussional syndrome then and now. Aust N Z J
Psychiatry 1988 Dec; 22(4): 396-402.
Sandel ME, Mysiw WJ: The agitated brain injured patient. Part 1: Definitions,
differential diagnosis, and assessment. Arch Phys Med Rehabil 1996 Jun; 77(6):
617-23.
Signorini DF, Alderson P: Therapeutic hypothermia for head injury. Cochrane
Database Syst Rev 2000; (2): CD001048.
Silver JM, Hales RE, Yudofsky S: Neuropsychiatric Aspects of Traumatic Brain
Injury. In: Textbook of Neuropsychiatry. 3rd ed. Washington, DC: American
Psychiatric Press; 1997: 521-60.
Skuster DZ, Digre KB, Corbett JJ: Neurologic conditions presenting as
psychiatric disorders. Psychiatr Clin North Am 1992 Jun; 15(2): 311-33.
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Florida Heart CPR*
Head Trauma Dementia Assessment
1. _____ describes the mental state of patients immediately following closed head
injury (CHI) or after awakening from coma. It is a form of delirium that may
persist for hours to weeks or, occasionally, months.
a. Posttraumatic amnesia
b. Posttraumatic thalamic syndrome
c. Postconcussive or postconcussional syndrome
d. Posttraumatic stress disorder
2. In this condition, the person progresses from generalized numbness to episodes
of spontaneous pain or pain in response to non-noxious stimuli.
a. Posttraumatic amnesia
b. Posttraumatic thalamic syndrome
c. Postconcussive or postconcussional syndrome
d. Posttraumatic stress disorder
3. This occurs when someone not yet fully recovered from a head injury
experiences another head or upper body injury, even seemingly trivial injury.
After a brief delay, the person suddenly loses consciousness. Signs of brainstem
compression follow, leading to death or permanent coma.
a. Posttraumatic thalamic syndrome
b. SIDS
c. SIS
d. Postconcussive or postconcussional syndrome
4. This syndrome follows mild-to-moderate CHI and produces significant disability.
The manifestations of this syndrome include irritability, fatigue, headaches,
dizziness, sensitivity to noise, cognitive slowing, memory impairment, poor
concentration, sadness, and anxiety.
a. Posttraumatic amnesia
b. Postconcussive or postconcussional syndrome
c. SIS
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d. Post traumatic thalamic syndrome
5. DAI, by definition, affects white matter. Personality remains relatively intact
unless other brain areas also are affected. In dementia from white matter injury,
cognitive impairment is ______.
a. Mild but progresses quickly
b. Mild and progresses slowly
c. Severe and progresses quickly
d. Severe but progresses slowly
6. The natural history of PCS follows a time course somewhat similar to that of
dementia from head injury. Rapid improvement typically occurs within the first
___month(s). However, impairments may persist a year or more.
a. 1
b. 2
c. 6
d. 10
7. Patients treated for sequelae of head injury should be screened for the
development or recurrence of any major psychiatric syndrome, including specific
screening for the following:
a. Mania
b. Anxiety
c. Depression
d. All of the above
8. Roughly ___% of head injuries in civilian populations are associated with alcohol
abuse.
a. 10
b. 25
c. 50
d. 75
9. In children, ______ are a significant cause of head injury.
a. Car accidents
b. Abusive siblings
c. Bicycle accidents
d. All of the above
10. Psychotropic medication may be useful in treating:
a. Mania
b. Anxiety
c. Insomnia
d. All of the above
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Florida Heart CPR*
Head Trauma Dementia